AD is a drifting brain degenerative disease, also known as a degenerative senile dementia, which is one of the most common and incurable dementia. AD occurs in the elderly, where older people have higher opportunities to get sick and people older than 85 years old have a 30˜35% prevalence rate. This progressive disease has its main clinical manifestations of degradation in three areas, including cognition, behavior and mental state. It has a special change in neuropathology, where some phenomena can be seen with naked eyes, like atrophy on appearance of cerebral cortex, widening of brain's back groove, and ventricular enlargement. Among them, most important pathological diagnostic indicators for AD are neurofibrillary tangles (NFT) and senile plaques (SP), which are widely distributed in neocortex. NFT is a result of windings of paired helical filaments of abnormal phosphorylated tau protein, which causes the formation of neurofibrillary tangles inside nerve cells. SPs are compositions of amyloid, where fibril deposits of Aβ protein are formed outside of nerve cells.
In recent researches, many small round precipitations or plaques are found in brains of AD patients. These spider web-like tangles of proteins are Aβ protein, which has become the focus on discussing AD mechanisms and treatments.
In prior studies, biological flags of AD can be divided into three categories, namely styrlbenzenes, like X-34, ISB, BSB, SB13 and IMSB; aminonaphthalene, like FDDNP and FENE; and thioflavin-S(TF-S), like 6-OH-BTA-1, TZDM and IMPY. Therein, FDDNP of aminonaphthalene is labeled with radioisotope fluorine(F)-18 to become F-18-FDDNP to be used as a contrast agent for positron emission tomography (PET).
In recent years, an increasing number of radiopharmaceuticals for Aβ protein plaques in positron CT scan have been developed and proven the feasibility of application on human body imaging. The use of the radiopharmaceuticals for tracing Aβ protein plaques can effectively assist in diagnosis of AD and related brain diseases, and can be used to evaluate effectiveness of the treatment drug for reducing accumulation of Aβ protein plaque in brain. But, a radiocontrast agent selectively and strongly bound to Aβ protein plaques to be used in PET imaging for AD and related brain diseases; or, to inhibit Aβ protein plaques for stopping the proceeding of AD and related brain disease, is still not found.
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